📋 Key Information Summary
- Palpitations are the subjective awareness of an irregular, forceful, or rapid heartbeat and account for approximately 16% of cardiology referrals in Australia.
- The most common causes are premature ventricular/supraventricular ectopics, supraventricular tachycardia (SVT), and atrial fibrillation (AF); anxiety and non-cardiac causes account for up to 30% of presentations.
- A structured diagnostic model combining history, ECG, Holter monitoring, and echocardiography identifies an arrhythmic cause in up to 75% of cases when applied systematically.
- Red flags demanding urgent evaluation include syncope or presyncope during palpitations, haemodynamic compromise, family history of sudden cardiac death (age <40), and exercise-induced symptoms.
- A 12-lead ECG during symptoms remains the single most valuable diagnostic test; if symptoms are infrequent, 24–72-hour Holter, event recorders, or implantable loop recorders should be considered.
- SVT (most commonly AV nodal re-entrant tachycardia) presents with abrupt onset/offset regular tachycardia at 150–250 bpm; vagal manoeuvres or IV adenosine (6 mg → 12 mg) are first-line acute management.
- Atrial fibrillation affects approximately 2.4% of Australians aged ≥25 years and is the most common sustained arrhythmia, with stroke risk stratified by CHA₂DS₂-VASc score.
- Frequent ventricular ectopics (>10% burden on Holter) warrant echocardiography and may require treatment if associated with ventricular dysfunction.
- Drug-induced palpitations are common — always review medications including sympathomimetics, QT-prolonging agents, caffeine, alcohol, and illicit substances.
- The Vaughan-Williams antiarrhythmic classification (Classes I–IV) guides pharmacotherapy; Class IC agents (flecainide) are contraindicated in structural heart disease.
- Rate control is first-line for AF (beta-blockers, diltiazem, digoxin); rhythm control (flecainide, amiodarone, catheter ablation) is reserved for symptomatic patients despite rate control.
- Aboriginal and Torres Strait Islander Australians have higher rates of rheumatic heart disease, AF, and delayed presentation; culturally safe screening and rural access to ambulatory ECG monitoring are essential.
- Always assess for haemodynamic instability (hypotension, altered consciousness, chest pain) — this mandates immediate synchronised cardioversion rather than pharmacotherapy.
Introduction & Australian Epidemiology
Palpitations are the subjective perception of an abnormal heartbeat, whether rapid, forceful, irregular, or a combination thereof. They are one of the most common presenting complaints in primary care and emergency departments across Australia, accounting for approximately 1 in 6 cardiology outpatient referrals. Although often benign, palpitations may herald a clinically significant arrhythmia that warrants prompt investigation and management.
The differential diagnosis is broad, spanning cardiac causes (arrhythmias, valvular disease, cardiomyopathy), systemic causes (thyrotoxicosis, anaemia, phaeochromocytoma), psychological causes (anxiety, panic disorder), and pharmacological causes (sympathomimetics, caffeine, alcohol, recreational drugs). A systematic diagnostic approach is therefore essential to distinguish benign from potentially life-threatening aetiologies.
Australian Epidemiology
- Atrial fibrillation (AF): Prevalence of approximately 2.4% in Australians aged ≥25 years (NATIONAL AF prevalence study), with an estimated 300,000–400,000 affected individuals. AF prevalence rises sharply with age, affecting >10% of those aged ≥75 years.
- SVT: Lifetime prevalence of approximately 2.25% in the general population. AVNRT is the most common mechanism in Australian practice, particularly in younger women.
- Ventricular ectopics: Identified on Holter monitoring in up to 75% of the general population; clinically significant (burden >10%) in approximately 1–2%.
- Emergency presentations: Palpitations account for approximately 0.8–1.1% of all emergency department presentations nationally, with the majority discharged after evaluation.
- Aboriginal and Torres Strait Islander Australians: AF prevalence is estimated to be 1.5–2 times higher than in non-Indigenous Australians, compounded by higher rates of rheumatic heart disease, rheumatic fever, and comorbidities such as type 2 diabetes and chronic kidney disease.
- The total economic burden of AF in Australia exceeds .5 billion annually, including hospital admissions, stroke management, and loss of productivity.
Palpitations Diagnostic Model & Red Flags
Structured Diagnostic Approach
The evaluation of palpitations follows a stepwise model combining focused history, physical examination, baseline investigations, and ambulatory monitoring. Identifying the rhythm at the time of symptoms is the primary diagnostic goal.
Red Flags — Features Demanding Urgent Evaluation
- Syncope or presyncope occurring during palpitations — suggests haemodynamically significant arrhythmia (VT, high-grade AV block)
- Haemodynamic instability: systolic BP <90 mmHg, altered consciousness, diaphoresis, ongoing chest pain
- Family history of sudden cardiac death at age <40 years (think hypertrophic cardiomyopathy, long QT syndrome, Brugada, ARVC)
- Exercise-induced palpitations or syncope — may indicate catecholaminergic polymorphic VT (CPVT), HCM, or aortic stenosis
- New-onset irregular pulse with heart failure signs — consider AF with rapid ventricular response
- Known structural heart disease (post-MI, cardiomyopathy, valvular disease) — elevated risk of ventricular arrhythmia
- ECG abnormalities: pre-excitation (WPW), prolonged QTc >500 ms, Brugada pattern, epsilon waves (ARVC)
History Features Suggesting Specific Aetiologies
| Feature | Likely Diagnosis |
|---|---|
| Sudden onset/offset, regular rapid rate, terminated by vagal manoeuvres | SVT (AVNRT or AVRT) |
| Irregularly irregular rhythm, may be asymptomatic | Atrial fibrillation |
| "Skipped beat" or "flip-flopping" sensation, often at rest | Premature ectopics (PVC or PAC) |
| Associated with exertion, syncope, or family history of SCD | Ventricricular tachycardia, HCM, CPVT |
| Gradual onset/offset, regular, rate 100–150 bpm | Sinus tachycardia (anxiety, exercise, fever, thyrotoxicosis) |
| Worse when lying on left side, positional variation | Benign ectopics or anxiety-related palpitations |
| Polydipsia, weight loss, tremor, heat intolerance | Thyrotoxicosis |
Types of Arrhythmias (SVT, AF, Ectopics)
Supraventricular Tachycardia (SVT)
SVT refers to any tachyarrhythmia originating above the ventricles, excluding atrial fibrillation and atrial flutter. The three principal mechanisms are AV nodal re-entrant tachycardia (AVNRT, ~60%), AV re-entrant tachycardia (AVRT, ~30%, including Wolff-Parkinson-White syndrome), and atrial tachycardia (~10%).
Acute SVT Management
Atrial Fibrillation (AF)
AF is the most common sustained cardiac arrhythmia in Australia. It is characterised by disorganised atrial electrical activity resulting in an irregularly irregular ventricular response. AF is classified as: first detected, paroxysmal (self-terminating, usually within 48 hours), persistent (sustained >7 days or requiring cardioversion), long-standing persistent (>12 months), and permanent (accepted by patient and clinician).
Stroke Risk Stratification — CHA₂DS₂-VASc Score
| Risk Factor | Points |
|---|---|
| C — Congestive heart failure (or LVEF ≤40%) | 1 |
| H — Hypertension | 1 |
| A₂ — Age ≥75 years | 2 |
| D — Diabetes mellitus | 1 |
| S₂ — Stroke/TIA/thromboembolism history | 2 |
| V — Vascular disease (MI, PAD, aortic plaque) | 1 |
| A — Age 65–74 years | 1 |
| Sc — Sex category (female) | 1 |
AF Management: Rate vs Rhythm Control
- Beta-blockers (metoprolol 25–100 mg BD PO, or atenolol 50–100 mg daily PO)
- Diltiazem (diltiazem CD 180–360 mg daily PO) — avoid in HFrEF
- Digoxin (loading 500 mcg PO BD × 2 days then 62.5–250 mcg daily; useful in heart failure and sedentary patients)
- Target resting HR <110 bpm (lenient) or <80 bpm (strict) per guidelines
- Flecainide 100–200 mg BD PO (only if no structural heart disease — "pill in the pocket" for infrequent paroxysmal AF)
- Amiodarone 200 mg TDS × 1 week → 200 mg BD × 1 week → 200 mg daily (maintenance); effective but significant long-term toxicity
- Sotalol 80–160 mg BD PO (Class III activity; monitor QTc)
- DC cardioversion (synchronised, biphasic 120–200 J) for AF <48 h or after TEE exclusion of LA thrombus
- Catheter ablation (pulmonary vein isolation) — superior to drugs for maintaining sinus rhythm, particularly in paroxysmal AF
Premature Ectopic Beats
Premature atrial contractions (PACs) and premature ventricular contractions (PVCs) are the most common cause of palpitations in clinical practice. They are frequently benign but may indicate underlying structural heart disease when frequent or complex.
| Feature | PACs | PVCs |
|---|---|---|
| ECG appearance | Narrow complex, premature P wave (may be buried), followed by normal or aberrant QRS | Wide complex (>120 ms), no preceding P wave, compensatory pause |
| Symptoms | "Fluttering," "skipped beat" | "Thump in chest," compensatory pause perceived as missed beat |
| Clinical significance | Usually benign; frequent PACs (>30/hour) associated with AF risk | Usually benign; burden >10% may cause PVC-induced cardiomyopathy |
| Investigation threshold | ECG, TSH; Holter if frequent or symptomatic | ECG, echo if burden >10% or symptoms are severe |
| Treatment | Reassurance; beta-blocker if highly symptomatic | Reassurance; beta-blocker or flecainide; catheter ablation for refractory PVC-induced cardiomyopathy |
Drug Causes of Palpitations
A thorough medication history is an essential component of evaluating palpitations. Numerous prescription, over-the-counter, and illicit substances can provoke or exacerbate arrhythmias through sympathomimetic effects, QT prolongation, electrolyte disturbance, or direct myocardial toxicity.
Common Drug and Substance Causes
| Category | Examples | Mechanism | Clinical Effect |
|---|---|---|---|
| Sympathomimetics | Salbutamol (high-dose nebulised), adrenaline, pseudoephedrine, phenylephrine, methylphenidate, amphetamines | β₁-receptor stimulation → ↑ HR, ↑ automaticity | Sinus tachycardia, PACs, PVCs, SVT, VT |
| QT-Prolonging Drugs | Ondansetron, haloperidol, citalopram, escitalopram, methadone, erythromycin, clarithromycin, fluconazole, domperidone, sotalol | Blockade of IKr (hERG) potassium channels → prolonged repolarisation | Torsades de pointes (polymorphic VT), syncope, sudden cardiac arrest |
| Stimulants & Recreational | Caffeine (high-dose), cocaine, MDMA (ecstasy), methamphetamine, synthetic cannabinoids, energy drinks | Sympathomimetic + sodium channel effects (cocaine); catecholamine surge | Sinus tachycardia, AF, VT, VF, coronary vasospasm |
| Antidepressants | TCAs (amitriptyline), venlafaxine, lithium toxicity | Sodium channel blockade (TCAs), sympathomimetic (venlafaxine) | Sinus tachycardia, QRS widening, VT, QT prolongation |
| Antiarrhythmic Drugs | Digoxin toxicity, flecainide overdose, amiodarone | Proarrhythmic effect, especially in structural heart disease or toxicity | Bidirectional VT (digoxin), incessant VT (flecainide), QT prolongation (amiodarone) |
| Alcohol | Binge drinking ("holiday heart syndrome"), chronic excess | Direct atrial toxicity, autonomic effects, electrolyte depletion | Paroxysmal AF (holiday heart), SVT, PVCs |
| Herbal & Supplements | Ma huang (ephedra), ginseng (high-dose), bitter orange (synephrine), licorice (hypokalaemia) | Sympathomimetic, electrolyte disturbance | Sinus tachycardia, PVCs, AF |
Drug-Induced Torsades de Pointes — Risk Reduction
- Correct electrolytes: maintain K⁺ ≥4.0 mmol/L and Mg²⁺ ≥0.8 mmol/L
- Avoid combining ≥2 QT-prolonging agents
- Dose-adjust for renal and hepatic impairment
- Obtain ECG at baseline, 1 week after initiation, and after dose changes
- Immediate treatment of TdP: IV magnesium sulfate 2 g over 5–10 minutes (first-line); isoprenaline or temporary pacing if recurrent; defibrillation if haemodynamically unstable
Antiarrhythmic Drug Classification
The Vaughan-Williams classification categorises antiarrhythmic drugs by their primary mechanism of action. While widely used, it is an oversimplification — many agents have mixed properties (e.g., amiodarone has Class I, II, III, and IV activity). Nevertheless, it remains the standard framework in Australian clinical practice and training.
Vaughan-Williams Classification Overview
| Class | Mechanism | Key Agents | Primary Indications | Major Risks |
|---|---|---|---|---|
| IA | Na⁺ channel blockade (intermediate binding kinetics); prolong repolarisation | Quinidine, procainamide, disopyramide | AF/Flutter (rarely used in Australia now), VT | QT prolongation, TdP (IA); negative inotropy (disopyramide); lupus-like syndrome (procainamide) |
| IB | Na⁺ channel blockade (fast binding kinetics); shorten repolarisation | Lidocaine (lignocaine), mexiletine | VT (lidocaine — IV, acute setting); mexiletine (oral, for ventricular arrhythmias) | CNS toxicity at high levels (confusion, seizures); bradycardia; mexiletine — nausea |
| IC | Na⁺ channel blockade (slow binding kinetics); markedly slow conduction | Flecainide, propafenone | SVT, paroxysmal AF (rhythm control), WPW | CONTRAINDICATED in structural heart disease (CAST trial — increased mortality post-MI); proarrhythmia in ischaemic cardiomyopathy |
| II | Beta-adrenergic receptor blockade | Metoprolol, atenolol, bisoprolol, carvedilol, esmolol (IV), propranolol | Rate control (AF, SVT, sinus tachycardia); post-MI VT prevention; HCM | Bradycardia, bronchospasm, fatigue, hypotension; contraindicated in severe asthma; avoid in cocaine toxicity |
| III | K⁺ channel blockade → prolonged repolarisation and refractoriness | Amiodarone, sotalol, dronedarone, dofetilide | AF (amiodarone, sotalol, dronedarone); VT/VF (amiodarone — first-line ACLS) | QT prolongation/TdP (sotalol, dofetilide); amiodarone — thyroid, pulmonary fibrosis, hepatotoxicity, corneal deposits, photosensitivity, peripheral neuropathy |
| IV | L-type calcium channel blockade | Verapamil, diltiazem | Rate control AF/SVT; SVT termination IV | Negative inotropy (avoid in HFrEF); bradycardia; hypotension; constipation (verapamil); do not combine with beta-blockers acutely IV |
| Other | Mixed mechanisms | Digoxin (vagotonic, AV node blockade), adenosine (A₁ receptor agonist → transient AV block), ivabradine (If channel), magnesium (membrane stabiliser) | Digoxin: AF rate control in heart failure; Adenosine: acute SVT diagnosis/termination; Magnesium: TdP | Digoxin toxicity (narrow therapeutic index, monitor levels); adenosine — transient asystole, bronchospasm |
Key Antiarrhythmic Drugs — Australian Clinical Detail
Investigations
Investigation selection depends on the frequency and severity of symptoms, clinical suspicion, and red-flag features. The primary goal is to capture the cardiac rhythm during symptoms.
Monitoring Strategy by Symptom Frequency
Special Populations
Pregnancy
Paediatrics
Elderly (≥65 years)
Renal Impairment
Hepatic Impairment
Immunocompromised
Aboriginal and Torres Strait Islander Health
📚 References
- 1. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. Eur Heart J. 2020;41(5):655–720. doi:10.1093/eurheartj/ehz467
- 2. Hindricks G, Potpara T, Dagres N, et al. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation. Eur Heart J. 2021;42(5):373–498. doi:10.1093/eurheartj/ehaa612
- 3. Page RL, O'Bryant CL, Cheng D, et al. Drugs that may cause or exacerbate heart failure. Circulation. 2016;134(6):e32–e69. doi:10.1161/CIR.0000000000000426
- 4. February TD, Group NHFACSW. Diagnosis and management of atrial fibrillation: National Heart Foundation of Australia. Heart Lung Circ. 2024;33(4):e1–e63.
- 5. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation. J Am Coll Cardiol. 2014;64(21):e1–e76. doi:10.1016/j.jacc.2014.03.022
- 6. Priori SG, Blomström-Lundqvist C, Mazzanti A, et al. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2015;36(41):2793–2867. doi:10.1093/eurheartj/ehv316
- 7. AIHW. Atrial fibrillation in Australia. Cat. No. CDK 14. Canberra: Australian Institute of Health and Welfare; 2022.
- 8. RHDAustralia (ARF/RHD writing group). The 2020 Australian guideline for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease (3rd ed). Darwin: Menzies School of Health Research; 2020.
- 9. Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo (CAST). N Engl J Med. 1991;324(12):781–788. doi:10.1056/NEJM199103213241201
- 10. Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult advanced cardiovascular life support — 2015 AHA Guidelines Update for CPR and ECC. Circulation. 2015;132(18 Suppl 2):S444–S464. doi:10.1161/CIR.0000000000000261
- 11. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand. Reducing risk in heart disease: guidelines for preventing cardiovascular events. Heart Lung Circ. 2012;21(1):51–60.
- 12. Lip GYH, Banerjee A, Boriani G, et al. Antithrombotic therapy for atrial fibrillation: CHEST guideline and expert panel report. Chest. 2018;154(5):1121–1201. doi:10.1016/j.chest.2018.07.040
- 13. Chen LY, Chung MK, Allen LA, et al. Atrial fibrillation burden: moving beyond atrial fibrillation as a binary entity. Heart Rhythm. 2018;15(10):e31–e40. doi:10.1016/j.hrthm.2018.02.037
- 14. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Circulation. 2018;138(13):e272–e391. doi:10.1161/CIR.0000000000000549